During spermiogenesis, male mice undergo a complex nuclear-cytoplasmic remodeling process where round spermatids must: elongate their nuclei, eliminate their cytoplasm, and develop the acrosome and tail structures necessary for fertilization. During this process, the spermatid develops an F-actin containing cytoskeletal plate, the acroplaxome. Furthermore, the acroplaxome anchors the acrosomal vesicle to the nuclear lamina. Although it is also thought the acroplaxome may play a role in sperm head shaping, the mechanism whereby this is achieved is poorly understood. Herein we describe a mouse line with a mutation in nonmuscle myosin II-A (NM II-A), E1841K, found in human MYH9-related disease. In addition to modeling MYH9-related disease male mice homozygous for the mutation (AE1841K/AE1841K) are sterile. Histological analyses and transmission electron microscopy of the AE1841K/AE1841K mouse testes show severely impaired round spermatid elongation. In the aberrant spermatids, the acroplaxome fails to correctly extend the developing acrosome. In addition, there is also failure in coupling of the tail to the spermatid head. Moreover, immunofluorescence confocal microscopy of both wild type and mutant developing round spermatids shows localization NM II-A to the acroplaxome. However, the mutant NM II-A acroplaxome often shows an irregular wave-like appearance not seen in the wild type. These observations suggest wild type NM II-A is required for proper spermatid nuclear-cytoplasmic remodeling and male fertility, both previously unknown functions for NM II-A. We speculate that NM II-A may serve to regulate the tension on the marginal ring of the acroplaxome, which is necessary for normal elongation and differentiation of the sperm head. Although the mechanism whereby the NM II-A E1841K mutation affects the coupling of the sperm tail and head remains unclear, our observations suggest a previously unknown role for NM II-A in sperm head shaping and male fertility.